Lipoprotein Metabolism and Fattening in Poultry

Abstract

Because de novo fatty acid synthesis in birds takes place mainly in the liver, adipose tissue growth and subsequent fattening depend on the availability of plasma triglycerides, which are transported as components of lipoproteins. In growing birds, VLDL is the major transporter of triglycerides, and attempts to reduce excessive fatness in poultry have involved the control of VLDL metabolism. Lean and fat lines of chickens have been selected on the basis of either their abdominal fat content or plasma VLDL concentration. In both cases, hepatic lipogenesis or LPL activity in adipose tissue did not differ between lean and fat lines, and therefore they did not appear to be limiting factors of susceptibility to fattening. In contrast, hepatic secretion and plasma concentration of VLDL were always higher in fat chickens than in lean chickens. Thus, current methods of selection of broilers against excessive fatness are based on this direct relationship between plasma VLDL and adiposity. When hepatic lipogenesis exceeds the capacity of VLDL secretion, triglycerides accumulate in the liver, causing steatosis. Although fatty liver is associated with reduced egg production and increased mortality in laying hens, hepatic steatosis in overfed ducks and geese is of positive economic value, serving as the basis for “foie-gras” production. The balance between synthesis and secretion of VLDL is therefore the key point that regulates hepatic and extrahepatic fattening in poultry.